Q-omics provides the consensus-scored CDH16 profile across patient tissues and cancer cell-line models. CDH16 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, CDH16 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, CDH16 RNA expression shows 9,246 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KICH, KIRC, and TGCT as cancer lineages where CDH16 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for CDH16 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CDH16 survival associations across molecular data types. CDH16 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (8) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CDH16 RNA expression–survival associations across cancer types. High CDH16 expression shows unfavorable associations in MESO, THYM and BLCA, but favorable associations in KICH, KIRC and CESC. The KICH Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .002). Together, the overview and detailed table identify KICH as the clearest survival context for CDH16 RNA expression.
This table summarizes CDH16 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CDH16. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CDH16 shows lower tumor expression in KIRC, THCA, KIRP, LUAD and KICH and higher tumor expression in LIHC. The KIRC box plot shows higher CDH16 RNA expression in normal versus tumor tissue (log2 FC = −2.880, t-test p < 0.001).
This table shows molecular features associated with CDH16 in patient tissues and cancer cell lines. In patient samples, CDH16 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, CDH16 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and KIDNEY.
